Justice Department Finds a Pattern of Civil Rights Violations by the Ferguson Police Department
The Justice Department announced the findings of its two civil rights investigations related to Ferguson, Missouri, today. The Justice Department found that the Ferguson Police Department (FPD) engaged in a pattern or practice of conduct that violates the First, Fourth, and 14th Amendments of the Constitution. The Justice Department also announced that the evidence examined in its independent, federal investigation into the fatal shooting of Michael Brown does not support federal civil rights charges against Ferguson Police Officer Darren Wilson.
“As detailed in our report, this investigation found a community that was deeply polarized, and where deep distrust and hostility often characterized interactions between police and area residents,” said Attorney General Eric Holder. “Our investigation showed that Ferguson police officers routinely violate the Fourth Amendment in stopping people without reasonable suspicion, arresting them without probable cause, and using unreasonable force against them. Now that our investigation has reached its conclusion, it is time for Ferguson’s leaders to take immediate, wholesale and structural corrective action. The report we have issued and the steps we have taken are only the beginning of a necessarily resource-intensive and inclusive process to promote reconciliation, to reduce and eliminate bias, and to bridge gaps and build understanding.”
“While the findings in Ferguson are very serious and the list of needed changes is long, the record of the Civil Rights Division’s work with police departments across the country shows that if the Ferguson Police Department truly commits to community policing, it can restore the trust it has lost,” said Acting Assistant Attorney General Vanita Gupta of the Civil Rights Division. “We look forward to working with City Officials and the many communities that make up Ferguson to develop and institute reforms that will focus the Ferguson Police Department on public safety and constitutional policing instead of revenue. Real community policing is possible and ensures that all people are equal before the law, and that law enforcement is seen as a part of, rather than distant from, the communities they serve.”
Attorney General Holder first announced the comprehensive pattern or practice investigation into the Ferguson Police Department after visiting that community in August 2014, and hearing directly from residents about police practices and the lack of trust between FPD and those they are sworn to protect. The investigation focused on the FPD’s use of force, including deadly force; stops, searches and arrests; discriminatory policing; and treatment of detainees inside Ferguson’s city jail by Ferguson police officers.
In the course of its pattern or practice investigation, the Civil Rights Division reviewed more than 35,000 pages of police records; interviewed and met with city, police and court officials, including the FPD’s chief and numerous other officers; conducted hundreds of in-person and telephone interviews, as well as participated in meetings with community members and groups; observed Ferguson Municipal Court sessions, and; analyzed FPD’s data on stops, searches and arrests. It found that the combination of Ferguson’s focus on generating revenue over public safety, along with racial bias, has a profound effect on the FPD’s police and court practices, resulting in conduct that routinely violates the Constitution and federal law. The department also found that these patterns created a lack of trust between the FPD and significant portions of Ferguson’s residents, especially African Americans.
The department found that the FPD has a pattern or practice of:
Conducting stops without reasonable suspicion and arrests without probable cause in violation of the Fourth Amendment;
Interfering with the right to free expression in violation of the First Amendment; and
Using unreasonable force in violation of the Fourth Amendment.
The department found that Ferguson Municipal Court has a pattern or practice of:
Focusing on revenue over public safety, leading to court practices that violate the 14th Amendment’s due process and equal protection requirements.
Court practices exacerbating the harm of Ferguson’s unconstitutional police practices and imposing particular hardship upon Ferguson’s most vulnerable residents, especially upon those living in or near poverty.Minor offenses can generate crippling debts, result in jail time because of an inability to pay and result in the loss of a driver’s license, employment, or housing.
The department found a pattern or practice of racial bias in both the FPD and municipal court:
The harms of Ferguson’s police and court practices are borne disproportionately by African Americans and that this disproportionate impact is avoidable.
Ferguson’s harmful court and police practices are due, at least in part, to intentional discrimination, as demonstrated by direct evidence of racial bias and stereotyping about African Americans by certain Ferguson police and municipal court officials.
The findings are laid out in a 100-page report that discusses the evidence and what remedies should be implemented to end the pattern or practice. The findings include two sets of recommendations, 26 in total, that the Justice Department believes are necessary to correct the unconstitutional FPD and Ferguson Municipal Court practices. The recommendations include: changing policing and court practices so that they are based on public safety instead of revenue; improving training and oversight; changing practices to reduce bias, and; ending an overreliance on arrest warrants as a means of collecting fines.
The Justice Department will require that the recommendations and other measures be part of a court-enforceable remedial process that includes involvement from community stakeholders as well as independent oversight. The Justice Department has provided its investigative report to the FPD and in the coming weeks, the Civil Rights Division will seek to work with the City of Ferguson and the Ferguson community to develop and reach an agreement for reform, using the recommendations in the report as the starting point.
The federal criminal investigation into the fatal shooting of Michael Brown sought to determine whether the evidence from the events that led to Brown’s death was sufficient to prove, beyond a reasonable doubt, that Wilson’s actions violated federal civil rights laws that make it a federal crime for someone acting with law enforcement authority to willfully violate a person’s civil rights. As part of the investigation, federal authorities reviewed physical, ballistic, forensic, and crime scene evidence; medical reports and autopsy reports, including an independent autopsy performed by the U.S. Department of Defense Armed Forces Medical Examiner Service; Wilson’s personnel records; audio and video recordings; internet postings, and; the transcripts from the proceedings before the St. Louis County grand jury. Federal investigators interviewed purported eyewitnesses and other individuals claiming to have relevant information. Federal prosecutors and agents re-interviewed dozens of witnesses to evaluate their accounts and obtain more detailed information. FBI agents independently canvassed more than 300 residences to locate and interview additional witnesses.
The standard of proof is the same for all criminal cases: that the defendant committed the crime beyond a reasonable doubt. However, unlike state laws, federal criminal civil rights statutes do not have the equivalent of manslaughter or a statute that makes negligence a crime. Federal statutes require the government to prove that Officer Wilson used unreasonable force when he shot Michael Brown and that he did so willfully, that is, he shot Brown knowing it was wrong and against the law to do so. After a careful and deliberative review of all of the evidence, the department has determined that the evidence does not establish that Darren Wilson violated the applicable federal criminal civil rights statute. The family of Michael Brown was notified earlier today of the department’s findings.
Due to the high interest in this case, the department took the rare step of publicly releasing the closing memo in the case. The report details, in over 80 pages, the evidence, including evidence from witnesses, the autopsies and physical evidence from the analysis of the DNA, blood, shooting scene and ballistics. The report also explains the law as developed by the federal courts and applies that law to the evidence.
DOJ Report on Shooting of Michael Brown
Ferguson Police Department Report
Pattern and Practice Typography
Pattern and Practice Chart
Citation: Li F, Zhu C, Deng F-Y, Wong MCM, Lu H-X, Feng X-P (2017) Herpesviruses in etiopathogenesis of aggressive periodontitis: A meta-analysis based on case-control studies. PLoS ONE 12(10): e0186373. https://doi.org/10.1371/journal.pone.0186373
Editor: Bruno Verhasselt, Ghent University, BELGIUM
Received: March 22, 2016; Accepted: October 1, 2017; Published: October 16, 2017
Copyright: © 2017 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Data Availability: All relevant data are within the paper and its Supporting Information files.
Funding: This work was supported by National Natural Science Foundation of China (Project No. 81400496—Hai-Xia Lu) and National Natural Science Foundation of China (Project No. 81470737—Xi-Ping Feng).
Competing interests: The authors have declared that no competing interests exist.
Aggressive periodontitis (AgP), characterized by early age of onset and tendency for familial aggregation, generally affects young patients, who show early and rapid periodontal breakdown with disproportionate amount of dental plaque in the lesion sites . The etiopathogenesis of AgP involves complex interaction between multifarious microorganisms and the host immune system . Bacteria have long been proposed as the causative and most important agents in the course of periodontal disease. However, the periodontal tissue destruction in AgP is usually site-specific, bilaterally symmetrical, occasionally breakout, and self-limited. These typical clinical manifestations of AgP cannot be well explained by bacterial infection alone . Hence, scholars thought that pure bacterial aetiology of AgP may have been over-emphasised .
Herpesviruses have been implicated in the etiopathogenesis of human periodontal disease since 1990s. A meta-analysis trying to demonstrate the association between herpesviruses and chronic periodontitis have been published . The etiopathogenesis of AgP differs from chronic periodontitis and the association between herpesviruses and AgP is still unclear. Numerous studies have investigated the association between herpesviruses and AgP [6–16]. However, the results of these studies remained controversial. Some researchers believed that herpesviruses do play a role in the etiopathogenesis of AgP, whereas others do not. Nibali et al.  failed to detect herpesviruses in any of the subgingival plaque samples from patients with AgP. Saygun et al.  reported no significant difference in copy numbers of herpesviruses between patients with AgP and periodontally healthy individuals.
Hence, the present study was conducted aiming at clarifying the association between occurrence of herpesviruses and risk of AgP by performing a meta-analysis based on available case–control studies (patients with AgP versus periodontally healthy individuals).
Materials and methods
This study was in compliance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement guidelines (More details were shown in S1 File). A review protocol did not exist.
Fei Li and Ce Zhu conducted computerized search of PubMed and Embase databases in October 2015 to retrieve relevant case–control studies investigating the association between herpesviruses and AgP. Terms employed for literature retrieve included: (1) “virus”, “herpesvir*”, “EBV”, “CMV”, “HCMV”, “HHV”, “HSV”, “Epstein–Barr virus”, “cytomegalovirus”, “herpes simplex virus”, “Human herpesvirus”; and (2) “aggressive periodontitis”, “parodontopathy”, “periodontal disease”, “periodontal”, “paradontosis”. The literature search was performed on English-language articles without any other restrictions (Electronic search strategy of PubMed database was shown on S2 File). Furthermore, we conducted a manual search on the reference lists of the eligible articles.
Inclusion and exclusion criteria
Studies were considered eligible if they met the following inclusion criteria: (1) studies were designed as case–control studies (patients with AgP vs periodontally healthy controls); (2) studies investigated the association between herpesviruses and AgP; (3) study samples were collected from these locations: biopsy, subgingival plaque, or gingival crevicular fluid; (4) the methods for herpesviruses’ detection were as follows: polymerase chain reaction (PCR), nested PCR, multiplex PCR, or real-time PCR; (5) all participants in the case and control groups were systemically healthy; and (6) the original articles provided available data, or we can obtain available data from the authors by inquiring email.
Studies were excluded if they met the following exclusion criteria: (1) studies were not of case–control design; (2) participants with systemic disease were involved in the case and control groups; (3) study samples were collected from saliva; (4) no available data could be obtained; and (5) study population were duplicate.
Potential inclusion was considered by screening title and abstract of all retrieved articles. Then full text was obtained for possible qualified articles. The same two reviewers independently assessed full text according to inclusion and exclusion criteria, eligible studies were submitted for final inclusion.
Data extraction was conducted in duplicate from included studies by the same two reviewers. The extracted data included first author, publication year, race of the study population, gender, mean age, number of patients and controls, sampling method, sample type, method of sample analyse, and detection rate of each herpesvirus. Controversial issues were resolved through discussion. Authors were directly contacted if crucial data was missing in original articles.
The methodological quality of each studies were assessed independently by the same two reviewers using the Newcastle–Ottawa Scale (NOS) . Total quality scores of the NOS ranges from 0 points to 9 points. Meanwhile, a higher score manifested better methodological quality. Studies with 7 points or higher were considered to be of high quality.
All statistical analysis was carried out using RevMan version 5.1 (The Nordic Cochrane Centre, The Cochrane Collaboration, Copenhagen, Denmark) and STATA version 12.0 (StataCorp, College Station, TX, USA) software. We estimated ORs and corresponding 95% CIs to measure the association between herpesviruses and risk of AgP. We didn’t have the assumption that all studies share a common effect, thus random-effects model was determined for all the quantitative synthesises. Additionally, the stability of the quantitative synthesis was evaluated by sensitivity analysis. One study was omitted sequentially, then the calculated combined OR for the remaining studies were assessed. We explored potential publication bias by constructing funnel plots and plot asymmetry test. Egger’s funnel plot asymmetry test (linear regression method) was performed to investigate the publication bias. P value less than 0.05 was considered as statistically significant and all test were two-sided.
Description of the studies
The process of study selection was shown in Fig 1. 1179 records were initially identified from PubMed and Embase databases. 1035 records were left after duplicates removed. Moreover, we excluded 975 non-relevant records by screening title and abstract. Then full texts of the remaining 60 articles were assessed in detail. Twelve eligible studies were included for meta-analysis according to the inclusion and exclusion criteria. Articles excluded from this step and the exclusion reasons were presented in S1 Table. Characteristics of the included studies were summarised in Table 1. There are 322 AgP patients and 342 periodontally healthy controls in our meta-analysis. The quality assessment scores using the NOS were also shown in Table 1, all the included studies were considered to be of high quality (The details of the assessment of the quality of the studies by NOS was shown on S3 File).
Fig 1. Flow chart for the study selection process.
# Undefined diagnosis: The diagnosis of patients is not appropriate or not clear. * No case-control design: Study is not design as case-control style.
Forest plots of the association between occurrence of herpesviruses and risk of AgP were shown in Fig 2. Quantitative synthesis was conducted separately by herpesvirus type. Association between EBV and AgP was analysed in ten studies, comprising 296 AgP patients and 305 periodontally healthy controls. The overall result based on random-effects model showed a significance between EBV and risk of AgP (10 studies: p = 0.0008, OR = 6.11, 95% confidence interval CI = 2.13–17.51) (Fig 2A).
12 studies involving 322 AgP patients and 342 periodontally healthy controls were examined to investigate the association between HCMV and risk of AgP. The overall result based on random-effects model showed that HCMV was associated with significantly increased risk of AgP (p = 0.009, OR = 3.63, 95% CI = 2.15–6.13) (Fig 2B).
Four eligible studies were examined to investigate the association between HSV-1 and AgP risk. The overall result based on random -effects model showed that HSV-1 was associated with significantly increased risk of AgP (p<0.001, OR = 19.19, 95% CI = 4.16–79.06) (Fig 2C).
Two eligible studies were examined to investigate the association between HSV-2 and risk of AgP. The pooled OR was estimated based on random-effects model (p = 0.20, OR = 3.46, 95% CI = 0.51–23.51) (Fig 2D). The association between HSV-2 and AgP was inconclusive due to insufficient data.
Only one study included covered the association between HHV-7 and risk of AgP (OR = 1.09, 95% CI = 0.21–5.76). VZV, HHV-6, and HHV-8 haven’t been reported in included studies.
Fig 3 showed the sensitivity analysis results of the associations between EBV, HCMV, HSV-1 and AgP. We conducted sensitivity analysis by omitting one study each time. The overall results yielded consistent results. In other words, no single study changed the overall ORs significantly, proving that the results were reliable. For the number limitation of articles included, sensitivity analysis for rest members of the herpesvirus family were not assessed.
Publication bias was treatedusing Egger’s funnel plot asymmetry test (linear regression method) according to herpesvirus type. Significant publication bias for EBV was detected using Egger’s funnel plot asymmetry test (EBV: Egger’s test, p < 0.001) (Fig 4A). No significant publication bias was detected for HCMV (HCMV: Egger’s test, p = 0.332). For the number limitation of articles included, sensitivity analysis for rest members of the herpesvirus family were not assessed.
Aggressive periodontitis is a high-risk and multi-factor disease which would result in the early loss of human teeth. The conventional pure bacterial pathogenicity theory of periodontal diseases was somewhat too weak to cover all the manifestation of AgP. Since mid 1990s when herpesviruses emerging as putative pathogens in periodontal diseases , more and more evidence convince that the presence of herpesviruses in the periodontal environment is associated with the occurrence and severity of AgP [10, 12–15, 19]. And compared with other types of periodontal diseases, AgP seems to have a closer connection with herpesviruses. The typical clinical manifestation of AgP like little plaque formation at sites with rapid periodontium destruction could be better explained by alteration between active and latent periods of herpesvirus infection . However, most of the data supporting these views come from the same research team, and contradictory reports have also been published. Some groups have reported weak connection even opposite results between AgP and herpesviruses [9, 11, 19]. Therefore, it is necessary to give overall estimations on the association between herpesviruses and AgP based on existing research data.
Several recent reviews [4, 23–26] have summarized the published findings on interaction between herpesviruses and AgP. Nevertheless, no quantitative synthesis analysis have been reported. Hence, this meta-analysis may help to provide more convincible evidence. Twelve studies were included in current meta-analysis. In five of twelve studies, HCMV genomes were detected in >50% of infected sites [8, 10, 13, 19, 27], while two studies reported negative results in all the samples [9, 12]. Control groups generally showed a low frequency of virus detection [8, 11, 14–16, 21]. Nevertheless, two control group studies reported HCMV occurrence higher than 50% [12, 13], whereas four did not detect HCMV in any of the infected sites [9, 10, 19, 27]. As for the detection of EBV, three out of ten studies reported a detection frequency of >50% in the infected site of AgP patients [10, 12, 19]. The other seven studies only detected EBV genomes in <45% of infected sites [8, 9, 13–16, 21]. Studies on periodontally healthy volunteers generally reported a low detection frequency of EBV, except for one study that detected EBV genomes in >50% of infected sites . Only three included studies reported the occurrence of HSV, two of which detected HSV genomes in >50% of infected sites of AgP patients [14, 19], and in fewer sites in the periodontally healthy group.
All the included studies reported adequate definition for patients in case group. The diagnosis criteria for “aggressive periodontitis” was based on the 1999 Consensus Classification  except for the study by Michalowicz et al . This study was submitted to final inclusion because the diagnosis criteria for case group in this study was in accordance with the 1999 Consensus Classification.
From the current meta-analysis, we concluded that HCMV and HSV-1 have significant association with increased risk of AgP. Both sensitivity analysis and publication bias test showed that the overall estimates were comparatively robust. Nevertheless, the significant pooled OR from quantitative synthesis for EBV was inconclusive because of considerable publication bias was found. Insufficient evidence was obtained to support the association between HSV-2 and HHV-7 and AgP since only two eligible studies for HSV-2 and one for HHV-7 were included. Additional high-quality, large scale studies are needed to achieve an unprejudiced conclusion. The rest members of the herpesvirus family were not covered in the studies included in our meta-analysis.
The exact pathogenic mechanisms of herpesviruses in periodontitis remain unclear. To the best of our knowledge, herpesviruses intervene in the inflammatory process by altering the immune mechanism and immune response in direct or indirect ways. Herpesviruses may exert their pathogenicity by a direct effect on different cells in the periodontium, virus-induced alteration of host immune defences, and enhancement of virulence of pathogenic bacteria . Wara-Aswapati described a hypothesis that, HCMV plays a role in the pathogenesis of periodontal disease by the ability of its immediate early proteins to strongly transactivate IL-1β gene expression. The most popular view in recent years is the pathogenic synergy between periodontopathic bacteria and herpesviruses [23, 30]. Herpesvirus infection predisposes the periodontal tissues to secondary infections by altering the adherence, chemotaxis, phagocytosis and bactericidal activity of polymorphonuclear leucocytes . Also, periodontopathic bacteria might activate periodontal herpesviruses through inflammation-inducing factors. Recent studies found that Porphyromonas gingivalis has the potential to trigger EBV by increasing the activity of the BZLF1 gene, which encodes the key protein for the transition from latency to the lytic replication cycle [31, 32]. Another study found that the co-infection of Porphyromonas gingivalis and EBV increase the gingival crevicular fluid visfatin levels, which might stimulate the expression of matrix-degrading enzymes and the breakdown of periodontal tissues .
Several limitations should be acknowledged in our meta-analysis. First, significant heterogeneity was detected among included studies in quantitative synthesis for HCMV and HSV-1. This may be caused by the differences on participants (age, gender, ethnic groups), sampling methods (Paper point, Curette, Biopsies), sample type (Subgingival plaque) and analysis methods (PCR, nested PCR, realtime-PCR, Q-PCR). However, we were unable to conduct subgroup analysis owing limited data. The conclusions should be cautiously interpreted. Second, confounding effect of age exist as a challenging task, although we have extracted the participants’ age distributions from each included study. Third, all included studies were published in English, leading to the limitation of data source and possibility of publication bias. According to the results of Egger’s funnel plot and Begg’s rank correlation test, publication bias for EBV was considerable, which means the result for EBV and risk of AgP might be inconclusive. However, there was no observable publication bias for HCMV and HSV-1. Last, the conclusion of this study was based on 12 independent studies and 664 subjects, which might be insufficient to quantify the risk estimate reliably. Especially, only four studies were included for HSV-1, which might not sufficient enough for a robust result.
In conclusion, the results from the current meta-analysis suggest that HCMV and HSV-1 are associated with significantly increased risk of AgP. Sensitivity analysis showed similar results. There was no indication of publication bias for HCMV and HSV-1, substantiating the robustness of our findings. Nevertheless, significant publication bias was observed for EBV, and the significant overall OR for EBV was inconclusive. These findings should be interpreted cautiously in view of the considerable heterogeneity among the included studies concerning HCMV and HSV-1. This study might provide a better understanding of the association between herpesviruses and AgP. Future research should be conducted to investigate co-infection with herpesviruses and bacteria and associated host responses in the development of periodontitis.
- 1. Watanabe SA, Correia-Silva Jde F, Horta MC, Costa JE, Gomez RS. EBV-1 and HCMV in aggressive periodontitis in Brazilian patients. Brazilian oral research. 2007;21(4):336–41. pmid:18060261.
- 2. Thomasini RL, Bonon SH, Durante P, Costa SC. Correlation of cytomegalovirus and human herpesvirus 7 with CD3+ and CD3+ CD4+ cells in chronic periodontitis patients. Journal of periodontal research. 2012;47(1):114–20. pmid:21895663.
- 3. Slots J, Kamma JJ, Sugar C. The herpesvirus-Porphyromonas gingivalis-periodontitis axis. Journal of periodontal research. 2003;38(3):318–23. pmid:12753371.
- 4. Slots J. Herpesvirus periodontitis: infection beyond biofilm. Journal of the California Dental Association. 2011;39(6):393–9. pmid:21823497.
- 5. Zhu C, Li F, Wong MC, Feng XP, Lu HX, Xu W. Association between Herpesviruses and Chronic Periodontitis: A Meta-Analysis Based on Case-Control Studies. PloS one. 2015;10(12):e0144319. pmid:26666412; PubMed Central PMCID: PMC4677929.
- 6. Kamma JJ, Contreras A, Slots J. Herpes viruses and periodontopathic bacteria in early-onset periodontitis. Journal of clinical periodontology. 2001;28(9):879–85. pmid:11493359.
- 7. Slots J, Pallasch TJ. Dentists' role in halting antimicrobial resistance. Journal of dental research. 1996;75(6):1338–41. pmid:8831626.
- 8. Michalowicz BS, Ronderos M, Camara-Silva R, Contreras A, Slots J. Human herpesviruses and Porphyromonas gingivalis are associated with juvenile periodontitis. Journal of periodontology. 2000;71(6):981–8. pmid:10914802.
- 9. Nibali L, Atkinson C, Griffiths P, Darbar U, Rakmanee T, Suvan J, et al. Low prevalence of subgingival viruses in periodontitis patients. Journal of clinical periodontology. 2009;36(11):928–32. pmid:19811582.
- 10. Yapar M, Saygun I, Ozdemir A, Kubar A, Sahin S. Prevalence of human herpesviruses in patients with aggressive periodontitis. Journal of periodontology. 2003;74(11):1634–40. pmid:14682660.
- 11. Botero JE, Parra B, Jaramillo A, Contreras A. Subgingival human cytomegalovirus correlates with increased clinical periodontal parameters and bacterial coinfection in periodontitis. Journal of periodontology. 2007;78(12):2303–10. pmid:18052702.
- 12. Rotola A, Cassai E, Farina R, Caselli E, Gentili V, Lazzarotto T, et al. Human herpesvirus 7, Epstein-Barr virus and human cytomegalovirus in periodontal tissues of periodontally diseased and healthy subjects. Journal of clinical periodontology. 2008;35(10):831–7. pmid:18691217.
- 13. Imbronito AV, Okuda OS, Maria de Freitas N, Moreira Lotufo RF, Nunes FD. Detection of herpesviruses and periodontal pathogens in subgingival plaque of patients with chronic periodontitis, generalized aggressive periodontitis, or gingivitis. Journal of periodontology. 2008;79(12):2313–21. pmid:19053922.
- 14. Das S, Krithiga GS, Gopalakrishnan S. Detection of human herpes viruses in patients with chronic and aggressive periodontitis and relationship between viruses and clinical parameters. Journal of oral and maxillofacial pathology: JOMFP. 2012;16(2):203–9. pmid:22923891; PubMed Central PMCID: PMC3424935.
- 15. Sharma R, Padmalatha O, Kaarthikeyan G, Jayakumar ND, Varghese S, Sherif K. Comparative analysis of presence of Cytomegalovirus (CMV) and Epsteinbarr virus -1 (EBV-1) in cases of chronic periodontitis and aggressive periodontitis with controls. Indian journal of dental research: official publication of Indian Society for Dental Research. 2012;23(4):454–8. pmid:23257476.
- 16. Stein JM, Said Yekta S, Kleines M, Ok D, Kasaj A, Reichert S, et al. Failure to detect an association between aggressive periodontitis and the prevalence of herpesviruses. Journal of clinical periodontology. 2013;40(1):1–7. pmid:23163882.
- 17. Saygun I, Nizam N, Keskiner I, Bal V, Kubar A, Acikel C, et al. Salivary infectious agents and periodontal disease status. Journal of periodontal research. 2011;46(2):235–9. pmid:21261620.
- 18. Wells GA, Shea B, O’Connell D, Peterson J, Welch V, M Losos, et al. (2000) The Newcastle-Ottawa Scale (NOS) for assessing the quality of nonrandomized studies in meta-analyses. Available at http://www.ohri.ca/programs/clinical_epidemiology/nosgen.pdf.
- 19. Saygun I, Kubar A, Ozdemir A, Yapar M, Slots J. Herpesviral-bacterial interrelationships in aggressive periodontitis. Journal of periodontal research. 2004;39(4):207–12. pmid:15206912.
- 20. Kubar A, Saygun I, Yapar M, Ozdemir A, Slots J. Real-time PCR quantification of cytomegalovirus in aggressive periodontitis lesions using TaqMan technology. Journal of periodontal research. 2004;39(2):81–6. pmid:15009514.
- 21. Sharma S, Tapashetti RP, Patil SR, Kalra SM, Bhat GK, Guvva S. Revelation of Viral—Bacterial Interrelationship in Aggressive Periodontitis via Polymerase Chain Reaction: A Microbiological Study. Journal of international oral health: JIOH. 2015;7(9):101–7. pmid:26435627; PubMed Central PMCID: PMC4589701.
- 22. Feller L, Meyerov R, Lemmer J. The association between human herpes viruses and periodontal disease, part 2. SADJ: journal of the South African Dental Association = tydskrif van die Suid-Afrikaanse Tandheelkundige Vereniging. 2007;62(4):170, 2, 4. pmid:17907585.
- 23. Slots J. Periodontal herpesviruses: prevalence, pathogenicity, systemic risk. Periodontology 2000. 2015;69(1):28–45. pmid:26252400.
- 24. Slots J. Human viruses in periodontitis. Periodontology 2000. 2010;53:89–110. pmid:20403107.
- 25. Slots J. Herpesviral-bacterial synergy in the pathogenesis of human periodontitis. Current opinion in infectious diseases. 2007;20(3):278–83. pmid:17471038.
- 26. Ambili R, Preeja C, Archana V, Nisha KJ, Seba A, Reejamol MK. Viruses: are they really culprits for periodontal disease? A critical review. Journal of investigative and clinical dentistry. 2014;5(3):179–87. pmid:23447363.
- 27. Kubar A, Saygun I, Ozdemir A, Yapar M, Slots J. Real-time polymerase chain reaction quantification of human cytomegalovirus and Epstein-Barr virus in periodontal pockets and the adjacent gingiva of periodontitis lesions. Journal of periodontal research. 2005;40(2):97–104. pmid:15733143.
- 28. Armitage GC. Development of a classification system for periodontal diseases and conditions. Annals of periodontology / the American Academy of Periodontology. 1999;4(1):1–6. pmid:10863370.
- 29. Wara-Aswapati N, Boch JA, Auron PE. Activation of interleukin 1beta gene transcription by human cytomegalovirus: molecular mechanisms and relevance to periodontitis. Oral microbiology and immunology. 2003;18(2):67–71. Epub 2003/03/26. pmid:12654093.
- 30. Slots J. Herpesviral-bacterial interactions in periodontal diseases. Periodontology 2000. 2010;52(1):117–40. pmid:20017799.